All the pathological and physiological changes noted in the lungs of the newborn developing "Hyaline Membrane Disease" can be explained by an increase in capillary pressure, which we feel is produced by automatically mediated increased resistance at the level of the pulmonary venules. There is immediate vascular engorgement, followed by interstitial and intra-alveolar hemorrhage. The hemodynamic imbalance results in formation of interstitial and intra-alveolar edema. The transudated plasma protein causes inactivation of surfactant, leading to atalectasis, and directly is responsible for the appearance of "hyaline membranes". We postulate that this sequence follows an initial episode of cerebral hypoxia, resulting in the prolonged autonomic dysfunction. We plan to use a benign cerebral arterial perfusion technique of our design to subject the animal subject's brain to hypoxemia, hypercarbia, acidemia, or combinations, while maintaining normal cerebral flow rates. We will maintain systemic arterial pressure and "gas" composition within the normal ranges. We will determine those metabolic alterations that will induce the functional and anatomical changes in the lungs. This will be done for piglets and monkeys, full term and premature newborns delivered by Caesarian section. We plan to study the acute plasma protein changes as this pulmonary complication develops over a brief period of time. This may give insight into the plasma components that contribute to the intra-alveolar "hyaline membrane". Establishing the pathogenesis of the Respiratory Distress of the newborn, and possibly also of similar conditions of the adult, will provide a rational basis for development of effective prophylactic and therapeutic measures. These would be aimed at restoration of normal cerebral function, reversal of the autonomic effects upon the pulmonary venular bed, and/or neutralizing the effects of pulmonary capillary hypertension.